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Biomedical subjects

S Saksena

Publications and source records attributed to S Saksena.

At least 163 records · Page 9Linked to original sources
PubMed1989

Radiofrequency ablation of ventricular myocardium using active fixation and passive contact catheter delivery systems.

This study examined the qualitative and quantitative effects of radiofrequency energy using active fixation and passive contact catheter delivery systems on normal bovine atrium and ventricle and diseased human ventricle in vitro. Two active fixation (custom screw-in or suction electrode) catheters and two passive contact (custom ring or standard electrode) catheters were used with a 500 kHz radiofrequency current generator. Linear regression analysis between lesion dimensions and power output showed excellent correlation coefficients for all catheter delivery systems except the suction catheter. Lesion sizes also increased with duration of radiofrequency energy delivery at low power using the USCI quadripolar catheter. Lesion size in diseased human ventricle was considerably smaller than in the normal ventricle. Comparison of induced lesion dimensions using pulsed and continuous delivery modes showed only minor differences. Tissue impedance was relatively constant during energy delivery. Arcing was associated with a sudden increase in voltage and impedance and a sudden decline in current. This was most frequently observed at high power and with the suction electrode catheter. The use of high (50 W) power output and prolonged application (up to 180 seconds) in atrium and ventricle did not induce perforation. We conclude that a variety of catheter delivery systems can be used for effective radiofrequency energy delivery and ablation in atrial and ventricular myocardium in the pulsed or continuous mode. Impedance changes during radiofrequency ablation cannot be used to guide the extent of ablation but do detect arcing during the procedure.

Animals↗
PubMed1989

Efficacy of nadolol alone or in combination with a type IA antiarrhythmic drug in sustained ventricular tachycardia: a prospective study.

We examined the clinical efficacy and safety of intravenous nadolol acutely, as well as chronic nadolol alone or combined with a type IA antiarrhythmic drug in 19 patients with sustained ventricular tachycardia and heart disease, mean age 62 +/- 15 years, and mean left ventricular ejection fraction 39 +/- 8%. Patients underwent electrophysiological studies in the drug-free state (control), after intravenous nadolol (dose = 0.05 mg/kg), and oral nadolol (dose = 80 mg/day) for 5 days alone or in combination with a type IA antiarrhythmic drug. Electrocardiographic and electrophysiological effects as well as ventricular tachycardia induction at electrophysiological study were analyzed. Long-term therapy with oral nadolol alone or in combination with a type IA antiarrhythmic drug was evaluated in responders. Intravenous nadolol prolonged RR and QRS intervals but had no effect on PR and QTc intervals. Oral nadolol alone tended to prolong RR intervals (P = 0.08). Oral nadolol with type IA antiarrhythmic drug prolonged RR and QTc intervals (P less than 0.001). The mean right ventricular effective refractory period tended to prolong after intravenous nadolol alone (from 251 +/- 29 to 263 +/- 25 msec, P = 0.08). Oral nadolol and type IA antiarrhythmic drugs did not prolong right ventricular effective refractory period (P = 0.3). Eighteen patients had inducible sustained ventricular tachycardia at control electrophysiological study. After intravenous nadolol, ventricular tachycardia was no longer inducible in seven patients. Ventricular tachycardia did not recur and remained noninducible in two of six patients who tolerated oral nadolol alone. Mean right ventricular effective refractory period prolonged from baseline values (from 249 +/- 30 to 271 +/- 30 msec, P less than 0.02) in patients who became noninducible on intravenous nadolol. In patients who remained inducible, mean right ventricular effective refractory period remained unchanged (from 253 +/- 29 to 258 +/- 22 msec, P greater than 0.2). In nonresponders to intravenous or oral nadolol, oral nadolol, and type IA antiarrhythmic drug suppressed ventricular tachycardia induction in two of ten patients. During follow-up, three patients continued on oral nadolol alone (one patient) or oral nadolol and type IA antiarrhythmic drug (two patients). Adverse effects resulting in nadolol discontinuation occurred in five patients. Therefore, we concluded that intravenous nadolol is effective in acute suppression of inducible ventricular tachycardia in selected patients. Oral nadolol alone or in combination with type IA antiarrhythmic drug is infrequently effective and poorly tolerated by this patient population. In addition, electrophysiological studies on intravenous nadolol do not predict the outcome of oral nadolol therapy.

Anti-Arrhythmia Agents↗
PubMed1989

Initial clinical experience with endocardial defibrillation using an implantable cardioverter/defibrillator with a triple-electrode system.

We evaluated the early clinical performance of an implantable cardioverter/defibrillator with a nonepicardial lead system in patients with refractory ventricular tachycardia or ventricular fibrillation. Ten patients, mean age 67 years, mean left ventricular ejection fraction 35%, refractory to 5 +/- 2 antiarrhythmic drugs and with a history of prior cardiac surgery (7 patients), severe lung disease (2 patients), or renal failure (1 patient) underwent device and lead system implant. A tripolar electrode catheter with one sensing electrode and two defibrillating electrodes was placed in the right ventricular apex and a left thoracic submuscular patch electrode was used in an epicostal location. Defibrillation energy threshold was determined using dual- or triple-electrode configurations. Optimal patch electrode location was determined after temporary use of a cutaneous patch electrode prior to cardioverter/defibrillator implant. Electrophysiologic studies were performed before discharge and after 2 to 3 months to assess device function. Percutaneous insertion and placement of the electrode catheter was achieved in all patients. Defibrillation energy threshold testing was done using 1 to 4 (mean, 2.7) electrode configurations per patient and required 6 to 21 (mean, 13) ventricular fibrillation inductions and 8 to 56 (mean, 22) shocks per patient. In all patients, lowest reliable defibrillation energy threshold was obtained with a triple-electrode configuration (right ventricular common cathode with right atrial and thoracic patch as dual anodes) and bidirectional shocks (mean, 18 +/- 5 J). Optimal patch electrode position could be determined in 9 of 10 patients, and these 9 patients had cardioverter/defibrillator implant. Ventricular fibrillation termination with the first delivered shock at electrophysiologic study was documented in all patients. There was no perioperative mortality in device-implanted patients. Postoperative electrophysiologic studies before discharge (9 patients) and at 3 months (8 patients) continued to demonstrate successful defibrillation by the first device shock. During follow-up (range, 2 to 10 months; mean, 6 +/- 3 months), spontaneous device discharges occurred in 4 patients with inappropriate shocks due to electrode catheter fracture being documented in 1 patient. Antiarrhythmic drug therapy was withdrawn in 6 patients and reduced in 3 patients. We conclude, based on our preliminary experience, that an implantable cardioverter/defibrillator can be successfully used with a nonepicardial lead system for endocardial defibrillation in many patients. This lead system can be used with currently available pulse generators and should be considered at cardioverter/defibrillator implantation. It can be anticipated to reduce patient risk and hospital costs associated with this procedure.

Aged↗
PubMed1988

Implantation of a cardioverter/defibrillator without thoracotomy using a triple electrode system.

This article describes the implantation of an automatic implantable cardioverter/defibrillator in a 69-year-old man with coronary artery disease and recurrent sustained ventricular tachycardia without the need for a thoracotomy/sternotomy and epicardial electrodes. The patient underwent serial electrophysiological evaluation that revealed drug-refractory ventricular tachycardia. Surgical ablation was considered and rejected due to advanced, severe, pulmonary disease. A triple electrode system using two transvenous catheter electrodes and a submuscular patch electrode in the left midaxillary line was employed. A single shock was delivered simultaneously over two spatially distinct current pathways and reproducibly defibrillated ventricular fibrillation with energies less than or equal to 10 J. The automatic implantable cardioverter/defibrillator was implanted in the anterior abdominal wall and demonstrated reproducible termination of ventricular tachycardia and ventricular fibrillation.

Aged↗
PubMed1988

Sequential transvenous pacing and shock therapy for termination of sustained ventricular tachycardia.

Rapid ventricular pacing and transvenous shocks are both effective in terminating sustained ventricular tachycardia (VT) only in selected patients. We prospectively examined efficacy and safety of an algorithm for VT termination combining rapid ventricular pacing with low and moderate energy transvenous shocks in patients with sustained VT. Sixty-three VT episodes in 23 patients, mean age 64 +/- 12 years, were treated with the algorithm. Bursts of rapid ventricular pacing and transvenous shocks were delivered with a Medtronic 6880 catheter positioned in the right ventricular apex. VT episodes with cycle lengths greater than 270 msec (group A) were treated with sequential therapy with rapid ventricular pacing (90%, 80%, and 70% of VT cycle length), low energy transvenous shocks (0.5 to 2.7 J), and moderate energy (2.7 to 10 J) transvenous shocks. Rapid VT episodes with cycle lengths less than 270 msec (group B) were treated with moderate energy transvenous shocks directly. Forty-one of 48 (85%) VT episodes in group A and 6 of 15 (40%) VT episodes in group B were successfully terminated by this algorithm. There was no difference in clinical or arrhythmia characteristics between responders and nonresponders in either group A or group B to the algorithm. VT acceleration was observed in 12% of episodes in group A and in 47% of episodes in group B. We conclude that an algorithm combining rapid ventricular pacing with low and moderate energy transvenous shocks is effective for VT termination in episodes with a cycle length greater than 270 msec and can reduce the need for transthoracic cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Long-term efficacy and safety of beta-adrenergic receptor antagonists for supraventricular tachycardia.

The efficacy and safety of nadolol and atenolol, 2 new long-acting beta-adrenergic receptor antagonists, were evaluated in patients with recurrent supraventricular tachycardia (SVT). Intravenous and oral drug therapy was administered to patients with atrioventricular reentrant tachycardia and atrioventricular nodal reentrant tachycardia. Efficacy was judged on a short-term basis by programmed electrical stimulation and on a long-term basis by clinical parameters and serial ambulatory electrocardiographic recordings during long-term follow-up. In addition, the usefulness of programmed electrical stimulation to predict long-term efficacy was evaluated. Intravenous nadolol prevented induction of SVT in 6 of 8 (75%) patients with atrioventricular nodal reentrant tachycardia, and oral nadolol prevented induction of SVT in 5 of 6 (83%) responders to intravenous nadolol. No episodes of sustained SVT recurred in these 5 patients during follow-up. Intravenous nadolol also prevented induction of SVT in 2 of 17 (11%) patients with atrioventricular reentrant tachycardia. Both patients remained non-inducible during treatment with oral nadolol, and neither experienced recurrence of SVT during follow-up. Intravenous atenolol prevented induction of SVT in 5 of 6 (83%) patients with atrioventricular nodal reentrant tachycardia. Oral atenolol prevented induction of atrioventricular nodal reentrant tachycardia in 4 of 5 (80%) patients responding to intravenous atenolol, and none of these 4 patients experienced a clinical recurrence. Intravenous atenolol prevented induction of SVT in 1 of 4 (25%) patients with atrioventricular reentrant tachycardia. Oral atenolol prevented induction of SVT in this patient and the arrhythmia has not recurred during follow-up. During follow-up (1 to 37 months), drug tolerance and compliance have been excellent with a low incidence of adverse reactions (11%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Electrophysiologic effects, clinical efficacy and safety of intravenous and oral nadolol in refractory supraventricular tachyarrhythmias.

The electrocardiographic and electrophysiologic effects, clinical efficacy and safety of intravenous and oral nadolol therapy were examined in 34 patients with recurrent supraventricular tachyarrhythmias (SVT) undergoing electrophysiologic evaluation. Programmed electrical stimulation was performed in the control (drug-free) state, after infusion of intravenous nadolol (mean dose 0.09 +/- 0.03 mg/kg) and after chronic oral nadolol therapy in patients who responded to intravenous nadolol (mean dose 83 +/- 12 mg for 5 days). Intravenous nadolol administration prolonged mean sinus cycle length (p = 0.009), mean PR interval (p = 0.001) and mean AH interval (p = 0.001), with no significant electrophysiologic effects in the atrium, ventricle or accessory bypass tracts. Oral nadolol had similar electrocardiographic and electrophysiologic effects, but of lesser magnitude. Intravenous nadolol resulted in complete suppression of induced SVT in 78% of patients with sinus and atrioventricular nodal reentrant tachycardia and 11% of patients with atrioventricular (AV) reentrant tachycardia (p less than 0.001). Partial responses were frequent in intraatrial or AV reentrant tachycardia (37%). Oral nadolol suppressed induction of SVT in patients who responded to intravenous nadolol. Adverse reactions to intravenous and oral nadolol were infrequent--6% and 8%, respectively--and usually did not require drug withdrawal. Intravenous nadolol is highly effective in sinus and AV nodal reentrant tachycardia, and a successful electrophysiologic response to it predicts efficacy of long-term oral nadolol therapy. It has limited efficacy alone in AV reentrant tachycardia and should be considered in combination with other antiarrhythmic therapy in this type of SVT.

Administration, Oral↗
PubMed1987

Intraoperative mapping-guided argon laser ablation of malignant ventricular tachycardia.

Intraoperative mapping-guided laser ablation of arrhythmogenic myocardium was performed in 5 patients with refractory sustained ventricular tachycardia (VT). Using a 15-W argon laser coupled to a 300-mu optical fiber, a bloodless laser ventriculotomy was successfully performed in 4 patients with VT. Visually- and mapping-guided endocardial ablation of 7 VT morphologic patterns was performed. Five of the 7 sites of VT origin were unresectable using standard resection techniques. Postoperatively, spontaneous and inducible VT was suppressed in all patients (without antiarrhythmic drugs in 4 patients and with a previously ineffective drug 1 patient). Mean pulmonary capillary wedge pressure, cardiac index and left ventricular ejection fraction were unchanged (p greater than 0.2) from preoperative values. Mean maximal creatinine kinase-MB isoenzyme concentration was 139 +/- 75 IU. All patients were New York Heart Association functional class II at discharge. During follow-up, no spontaneous arrhythmia has recurred in any patient. Thus, intraoperative argon laser ablation is effective for VT ablation alone or in conjunction with standard surgical resection techniques.

Aged↗
PubMed1987

Management of refractory sustained ventricular tachycardia with amiodarone: a reappraisal.

We examined the value of clinical variables, chronic 24-hour ambulatory ECG monitoring, and chronic electrophysiologic (EP) testing in 49 patients with recurrent and refractory sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) treated with chronic oral amiodarone in order to develop a prospective approach to the management of these patients. All patients underwent control EP studies followed by continuous telemetric cardiac monitoring during oral amiodarone administration (mean duration 29 +/- 6 days, mean dose 739 +/- 230 mg). Follow-up 24-hour ambulatory ECG monitoring and EP studies were performed. Thirty VT recurrences occurred in the first 4 weeks of amiodarone therapy (total incidence, 61%), with the majority (55%) in the first 3 weeks of treatment. During long-term follow-up (1 to 42, mean 15 +/- 12 months), there were 12 symptomatic VT/VF recurrences (incidence 24%). There was a higher incidence of VT recurrences if patients had inducible sustained or nonsustained VT at chronic EP study (p less than 0.01), or complex ventricular arrhythmias on ambulatory ECG monitoring (p less than 0.05). The sensitivity, specificity, and predictive accuracy of chronic EP testing and 24-hour ambulatory ECG monitoring were 100%, 35%, and 51%, and 58%, 84%, and 78%, respectively. Chronic EP testing correctly identified all patients who had their arrhythmia suppressed by amiodarone on long-term follow-up, while 42% of all VT recurrences occurred in patients without complex ventricular arrhythmias on 24-hour ambulatory ECG monitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Mechanisms of ventricular tachycardia termination and acceleration during transvenous cardioversion as determined by cardiac mapping in man.

We examined the EP mechanisms underlying efficacy and inefficacy of transvenous cardioversion shocks in 13 patients with coronary artery disease and sustained VT during preoperative and intraoperative cardiac mapping procedures. Shocks were delivered at the right ventricular apex with a Medtronic 6880 catheter and a Model 5350 external cardioverter/defibrillator with two or three electrode configurations, resulting in unidirectional or bidirectional shocks, respectively. Single transvenous shocks with incremental energies ranging from 0.03 to 25 J were delivered in sinus rhythm and VT, and simultaneous right and left ventricular electrograms were obtained. Transvenous cardioversion shocks of 0.03 J in sinus rhythm and VT produced immediate local right ventricular depolarization and subsequently conducted to distant right ventricular and left ventricular sites after 30 to 100 msec. Shocks of 0.05 to 0.5 J produced immediate depolarization of progressively larger right ventricular and left ventricular regions, with shocks greater than or equal to 0.5 J producing immediate depolarization of distant left ventricular sites in sinus rhythm. High energy (greater than 5 J) shocks produced instantaneous depolarization of multiple right ventricular and left ventricular sites in VT. VT termination occurred due to either delay or interruption of conduction in the tachycardia circuit, despite prior depolarization of the early sites of ventricular activation during the QRS complex. This could be due to instantaneous or paced depolarization of critical "excitable" components of the VT circuit, resulting either in immediate conduction block or in instability followed by termination. VT acceleration with transvenous cardioversion was due to modification of the "excitable," slowly conducting components of the VT circuit with the development of new areas of conduction block, along with altered intraventricular conduction. Similar EP mechanisms were observed with unidirectional and bidirectional transvenous shock patterns. We conclude that transvenous shocks alter conduction in human ventricle, and clinical effects of QRS synchronized shocks are related to conduction changes induced in the excitable components of the VT circuit.

Aged↗